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Case-only study of interactions between genetic polymorphisms of GSTM1, P1, T1 and Z1 and smoking in Parkinson's disease.
Neurosci Lett. 2004 Aug 19; 366(3):326-31.NL

Abstract

Current opinion contends that complex interactions between genetic and environmental factors play a role in the etiology of Parkinson's disease (PD). Cigarette smoking is thought to reduce risk of PD, and emerging evidence suggests that genetic factors may modulate smoking's effect. We used a case-only design, an approach not previously used to study gene-environment interactions in PD, specifically to study interactions between glutathione-S-transferase (GST) gene polymorphisms and smoking in relation to PD. Four-hundred PD cases (age at onset: 60.0 +/- 10.7 years) were genotyped for common polymorphisms in GSTM1, P1, T1 and Z1 using well-established methods. Smoking exposure data were collected in face-to-face interviews. The independence of the studied GST genotypes and smoking exposure was confirmed by studying 402 healthy, aged individuals. No differences were observed in the distributions of GSTM1, T1 or Z1 polymorphisms between ever-smoked and never-smoked PD cases using logistic regression (all P > 0.43). However, GSTP1 *C haplotypes were over-represented among PD cases who ever smoked (odds ratio for interaction (ORi) = 2.00 (95% CI: 1.11-3.60, P = 0.03)). Analysis revealed that ORi between smoking and the GSTP1-114Val carrier status increased with increasing smoking dose (P = 0.02 for trend). These data suggest that one or more GSTP1 polymorphisms may interact with cigarette smoking to influence the risk for PD.

Authors+Show Affiliations

Centre for Health Research, School of Public Health, Queensland University of Technology, Kelvin Grove, Qld. 4059, Australia.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15288444

Citation

Deng, Yifu, et al. "Case-only Study of Interactions Between Genetic Polymorphisms of GSTM1, P1, T1 and Z1 and Smoking in Parkinson's Disease." Neuroscience Letters, vol. 366, no. 3, 2004, pp. 326-31.
Deng Y, Newman B, Dunne MP, et al. Case-only study of interactions between genetic polymorphisms of GSTM1, P1, T1 and Z1 and smoking in Parkinson's disease. Neurosci Lett. 2004;366(3):326-31.
Deng, Y., Newman, B., Dunne, M. P., Silburn, P. A., & Mellick, G. D. (2004). Case-only study of interactions between genetic polymorphisms of GSTM1, P1, T1 and Z1 and smoking in Parkinson's disease. Neuroscience Letters, 366(3), 326-31.
Deng Y, et al. Case-only Study of Interactions Between Genetic Polymorphisms of GSTM1, P1, T1 and Z1 and Smoking in Parkinson's Disease. Neurosci Lett. 2004 Aug 19;366(3):326-31. PubMed PMID: 15288444.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Case-only study of interactions between genetic polymorphisms of GSTM1, P1, T1 and Z1 and smoking in Parkinson's disease. AU - Deng,Yifu, AU - Newman,Beth, AU - Dunne,Michael P, AU - Silburn,Peter A, AU - Mellick,George D, PY - 2004/03/19/received PY - 2004/05/20/revised PY - 2004/05/22/accepted PY - 2004/8/4/pubmed PY - 2004/10/9/medline PY - 2004/8/4/entrez SP - 326 EP - 31 JF - Neuroscience letters JO - Neurosci Lett VL - 366 IS - 3 N2 - Current opinion contends that complex interactions between genetic and environmental factors play a role in the etiology of Parkinson's disease (PD). Cigarette smoking is thought to reduce risk of PD, and emerging evidence suggests that genetic factors may modulate smoking's effect. We used a case-only design, an approach not previously used to study gene-environment interactions in PD, specifically to study interactions between glutathione-S-transferase (GST) gene polymorphisms and smoking in relation to PD. Four-hundred PD cases (age at onset: 60.0 +/- 10.7 years) were genotyped for common polymorphisms in GSTM1, P1, T1 and Z1 using well-established methods. Smoking exposure data were collected in face-to-face interviews. The independence of the studied GST genotypes and smoking exposure was confirmed by studying 402 healthy, aged individuals. No differences were observed in the distributions of GSTM1, T1 or Z1 polymorphisms between ever-smoked and never-smoked PD cases using logistic regression (all P > 0.43). However, GSTP1 *C haplotypes were over-represented among PD cases who ever smoked (odds ratio for interaction (ORi) = 2.00 (95% CI: 1.11-3.60, P = 0.03)). Analysis revealed that ORi between smoking and the GSTP1-114Val carrier status increased with increasing smoking dose (P = 0.02 for trend). These data suggest that one or more GSTP1 polymorphisms may interact with cigarette smoking to influence the risk for PD. SN - 0304-3940 UR - https://www.unboundmedicine.com/medline/citation/15288444/Case_only_study_of_interactions_between_genetic_polymorphisms_of_GSTM1_P1_T1_and_Z1_and_smoking_in_Parkinson's_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304394004006561 DB - PRIME DP - Unbound Medicine ER -